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Mol Immunol. 2008 Jun;45(11):3230-7. doi: 10.1016/j.molimm.2008.02.020. Epub 2008 Apr 9.

Role of STAT3 in glucocorticoid-induced expression of the human IL-10 gene.

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Clinical Cooperation Group, Inflammatory Lung Diseases, Helmholtz Zentrum M√ľnchen, German Research Center for Environmental Health and Asklepios-Fachklinik, Robert-Koch-Allee 29, 82131 Gauting, Germany.


In the present report we have determined the molecular mechanisms, which govern the expression of the human IL-10 gene when induced by the glucocorticoid Methyl-Prednisolone (MP). Treatment of cells with MP at 10(-6) M will readily induce IL-10 in CD19+ primary B cells and in a human B cell line. Analysis of the IL-10 promoter showed a robust 18-fold induction and demonstrated that a potential GRE motif was not required, while mutation of the -120 STAT-motif strongly reduced MP-induced trans-activation. A strong induction was also seen with a trimeric STAT-motif and over-expression of dominant-negative STAT3 could block MP induction of IL-10 mRNA. Finally, MP treatment induced binding of STAT3 to the promoter as shown by gelshift, supershift and by chromatin-immunoprecipitation. These data show that glucocorticoid-induced expression of the IL-10 gene is mediated by the transcription factor STAT3.

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